Interaction of a Novel Alternatively Spliced Variant of HSD11B1L with Parkin Enhances the Carcinogenesis Potential of Glioblastoma: Peiminine Interferes with This Interaction
Abstract:Glioblastoma (GBM) is a primary brain tumor of unknown etiology. It is extremely aggressive, incurable and has a short average survival time for patients. Therefore, understanding the precise molecular mechanisms of this diseases is essential to establish effective treatments. In this study, we cloned and sequenced a splice variant of the hydroxysteroid-like 11-β dehydrogenase 1 gene (HSD11B1L) and named it HSD11B1L-181. HSD11 B1L-181 was specifically expressed only in GBM cells. Overexpression of this variant… Show more
“…The overexpression of this variant was shown to notably enhance the proliferation, migration, and invasion of Glioblastoma (GBM) cells. Conversely, the suppression of HSD11B1L-181 expression resulted in the inhibition of the oncogenic potential of GBM cells 49 . These discoveries indicate the potential for targeting 11β-HSD1 as a valuable adjunct in cancer therapy.…”
This study aimed to investigate the diagnostic value of miR-451a, miR-5571-3p, CLN6, HSD11B1, and PDE4 as potential biomarkers for distinguishing patients with Granulomatous lobular mastitis (GLM), breast cancer (BC), and breast fibroadenoma. A total of 55 participants were included in each group. The serum expressions of miR-451a and miR-5571-3p were significantly higher in the GLM (0.95 ± 0.47, 7.20 ± 3.99) and control groups (0.21 ± 0.13, 1.74 ± 1.49) than in the BC group (p < 0.01). Meanwhile, the expression of miR-451a and miR-5571-3p in GLM was significantly higher than in the control group (0.21 ± 0.13, 1.74 ± 1.49; p < 0.001). The levels of CLN6 in the GLM(1.37 ± 0.87) and BC((1.57 ± 0.84) groups were higher than those in the control group (p < 0.001). Furthermore, HSD11B1 and PDE4 expressions were significantly increased in the BC (1.92 ± 1.14, 1.54 ± 0.88) and GLM (1.07 ± 0.70, 0.85 ± 0.51) groups compared to the control group (p < 0.01), with higher levels observed in the BC group than in the GLM group (p < 0.01). Taken together, these findings suggest that serum miR-451a, miR-5571-3p, and CLN6 may serve as noninvasive biomarkers for differentiating GLM, BC, and breast fibroadenoma. This study provides a basis for future investigations in the differential diagnosis of these breast diseases.
“…The overexpression of this variant was shown to notably enhance the proliferation, migration, and invasion of Glioblastoma (GBM) cells. Conversely, the suppression of HSD11B1L-181 expression resulted in the inhibition of the oncogenic potential of GBM cells 49 . These discoveries indicate the potential for targeting 11β-HSD1 as a valuable adjunct in cancer therapy.…”
This study aimed to investigate the diagnostic value of miR-451a, miR-5571-3p, CLN6, HSD11B1, and PDE4 as potential biomarkers for distinguishing patients with Granulomatous lobular mastitis (GLM), breast cancer (BC), and breast fibroadenoma. A total of 55 participants were included in each group. The serum expressions of miR-451a and miR-5571-3p were significantly higher in the GLM (0.95 ± 0.47, 7.20 ± 3.99) and control groups (0.21 ± 0.13, 1.74 ± 1.49) than in the BC group (p < 0.01). Meanwhile, the expression of miR-451a and miR-5571-3p in GLM was significantly higher than in the control group (0.21 ± 0.13, 1.74 ± 1.49; p < 0.001). The levels of CLN6 in the GLM(1.37 ± 0.87) and BC((1.57 ± 0.84) groups were higher than those in the control group (p < 0.001). Furthermore, HSD11B1 and PDE4 expressions were significantly increased in the BC (1.92 ± 1.14, 1.54 ± 0.88) and GLM (1.07 ± 0.70, 0.85 ± 0.51) groups compared to the control group (p < 0.01), with higher levels observed in the BC group than in the GLM group (p < 0.01). Taken together, these findings suggest that serum miR-451a, miR-5571-3p, and CLN6 may serve as noninvasive biomarkers for differentiating GLM, BC, and breast fibroadenoma. This study provides a basis for future investigations in the differential diagnosis of these breast diseases.
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